RANKL promotes the differentiation and activation of osteoclasts and stimulates and maintains their resorption activity.9,10 It has also been proposed that many osteoporotic pathways, such as those induced by cytokines or hormones, are primarily mediated by inducing RANKL expression in osteoblast lineage cells.7,8 Studies on mice revealed that the administration of soluble RANKL results in an increase in the formation and activation of osteoclasts that lead to osteoporosis.11 On the other hand, OPG is a potent inhibitor of osteoclast formation and acts as a decoy receptor for RANKL. Here, TNFSF11 is linked to osteoporosis.